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Alisol A Exerts Anti-Proliferative Activity against Human Oral Cancer Cells through Triggering JNK/p38 MAPK-Mediated
Yi-Tzu Chen1,2,3, Shao-Hsuan Kao4,5, Chun-Yi Chuang6,7
1School of Dentistry, Chung Shan Medical University, Taichung, 402, Taiwan.
Background:
Alisol A is a natural compound isolated from Alismatis Rhizoma, known for its diverse pharmacological activities, including anticancer and neuroprotective effects. This study aimed to explore the anticancer effects of Alisol A on oral cancer cells and elucidate its underlying mechanisms.
Methods:
Cell viability was measured by MTT assay, cell cycle by flow cytometry, and apoptosis by Annexin V/PI staining and caspase activation. Regulation of signaling pathways was analyzed using an apoptosis-related protein array, immunoblotting, and specific kinase inhibitors.
Results:
Alisol A reduced the viability of oral cancer cell lines, induced sub-G1 phase accumulation, and augmented the number of apoptotic cells. Protein array results indicated that Alisol A enhanced the expression of heme oxygenase-1 (HO-1), while suppressing cellular inhibitor of apoptosis protein 1 (cIAP1) and X-linked inhibitor of apoptosis protein (XIAP) levels in SCC-9 cells. These changes were further confirmed in both SCC-9 and HSC-3 cells by immunoblotting. In addition, Alisol A triggered the activation of caspase-8, -9, and -3, as well as poly (ADP-ribose) polymerase (PARP) cleavage in both cell lines. Analysis of signaling pathways showed that mitogen-activated protein kinases (MAPKs) were significantly activated by Alisol A. Notably, inhibition of JNK and p38 markedly reduced Alisol A-induced activation of caspase-8, -9, and -3.
Conclusions:
Our findings demonstrate that Alisol A exerts potent anticancer effects on oral cancer cells by inducing caspase-dependent apoptosis via activation of the JNK and p38 signaling pathways. These results suggest that Alisol A may have therapeutic potential for the treatment of oral cancer.
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